ReviewCurrent neuropharmacology2025
The Biological Changes of Synaptic Plasticity in the Pathological Process of Sepsis-associated Encephalopathy.
Review in Current neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Astrocytic LCN2 mediates pathological crosstalk with neurons to promote neuronal loss in sepsis-associated encephalopathy.Cell death and differentiation · 2026Article
- Impact of Chronic Mild Stress on Neurotrophic and Hypothalamic-Pituitary-Adrenal Factors in the Brain of Rats Submitted to Sepsis.Neurotoxicity research · 2026Article
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Targeting synaptic plasticity to bridge translational gaps in sepsis-associated encephalopathy.Frontiers in aging neuroscience · 2025Review
- The non-linear association between creatinine-to-albumin ratio and medium-term mortality in patients with sepsis accompanied by acute kidney injury in the intensive care unit: a retrospective study based on the MIMIC database and external validation.Frontiers in cellular and infection microbiology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Sepsis-associated encephalopathy (SAE) is a form of cognitive and psychological impairment resulting from sepsis, which occurs without any central nervous system infection or structural brain injury. Patients may experience long-term cognitive deficits and psychiatric disorders even after discharge. However, the underlying mechanism remains unclear. As cognitive function and mental disease are closely related to synaptic plasticity, it is presumed that alterations in synaptic plasticity play an essential role in the pathological process of SAE. Here, we present a systematic description of the pathogenesis of SAE, which is primarily driven by glial cell activation and subsequent release of inflammatory mediators. Additionally, we elucidate the alterations in synaptic plasticity that occur during SAE and comprehensively discuss the roles played by glial cells and inflammatory factors in this process. In this review, we mainly discuss the synaptic plasticity of SAE, and the main aim is to show the consequences of SAE on inflammatory factors and how they affect synaptic plasticity. This review may enhance our understanding of the mechanism underlying cognitive dysfunction and provide valuable insights into identifying appropriate therapeutic targets for SAE.
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